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N6-methyladenosine is the most common modification of eukaryotic RNA. N6-methyladenosine participates in RNA splicing, nuclear export, translation, and degradation through regulation by methyltransferases, methylation readers, and demethylases, affecting messenger RNA stability and translation efficiency. Through the dynamic and reversible regulatory network composed of "writers, erasers, and readers," N6-methyladenosine modification plays a unique role in the process of hematopoiesis. Acute myeloid leukemia is a heterogeneous disease characterized by malignant proliferation of hematopoietic stem cells/progenitor cells. Many studies have shown that N6-methyladenosine-related proteins are abnormally expressed in acute myeloid leukemia and play an important role in the occurrence and development of acute myeloid leukemia, acting as carcinogenic or anticancer factors. Here, we describe the mechanisms of action of reversing N6-methyladenosine modification in hematopoiesis and acute myeloid leukemia occurrence and progression to provide a basis for further research on the role of N6-methyladenosine methylation and its regulatory factors in normal hematopoiesis and acute myeloid leukemia, to ultimately estimate its potential clinical value.
Fang et al. (2024) studied this question.